Tissue-Specific Macrophage Responses to Remote Injury Impact the Outcome of Subsequent Local Immune Challenge.
Animals
Biomarkers
Cell Count
Disease Susceptibility
/ immunology
ErbB Receptors
/ metabolism
Gene Expression Profiling
Gene Expression Regulation
Gene Regulatory Networks
Ischemia
/ etiology
Macrophages
/ immunology
Macrophages, Alveolar
/ immunology
Mice
Muscle Cells
/ immunology
Myocardial Infarction
/ etiology
Organ Specificity
/ genetics
Pneumonia
/ etiology
macrophage
myocardial infarction
sepsis
stroke
Journal
Immunity
ISSN: 1097-4180
Titre abrégé: Immunity
Pays: United States
ID NLM: 9432918
Informations de publication
Date de publication:
19 11 2019
19 11 2019
Historique:
received:
01
10
2018
revised:
06
09
2019
accepted:
23
10
2019
pubmed:
17
11
2019
medline:
23
1
2020
entrez:
17
11
2019
Statut:
ppublish
Résumé
Myocardial infarction, stroke, and sepsis trigger systemic inflammation and organism-wide complications that are difficult to manage. Here, we examined the contribution of macrophages residing in vital organs to the systemic response after these injuries. We generated a comprehensive catalog of changes in macrophage number, origin, and gene expression in the heart, brain, liver, kidney, and lung of mice with myocardial infarction, stroke, or sepsis. Predominantly fueled by heightened local proliferation, tissue macrophage numbers increased systemically. Macrophages in the same organ responded similarly to different injuries by altering expression of tissue-specific gene sets. Preceding myocardial infarction improved survival of subsequent pneumonia due to enhanced bacterial clearance, which was caused by IFNɣ priming of alveolar macrophages. Conversely, EGF receptor signaling in macrophages exacerbated inflammatory lung injury. Our data suggest that local injury activates macrophages in remote organs and that targeting macrophages could improve resilience against systemic complications following myocardial infarction, stroke, and sepsis.
Identifiants
pubmed: 31732166
pii: S1074-7613(19)30454-6
doi: 10.1016/j.immuni.2019.10.010
pmc: PMC6892583
mid: NIHMS1543682
pii:
doi:
Substances chimiques
Biomarkers
0
EGFR protein, mouse
EC 2.7.10.1
ErbB Receptors
EC 2.7.10.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
899-914.e7Subventions
Organisme : NIAMS NIH HHS
ID : DP2 AR075321
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL125428
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK043351
Pays : United States
Organisme : NHLBI NIH HHS
ID : K99 HL129168
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM083016
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS084863
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK057521
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM053522
Pays : United States
Organisme : NHLBI NIH HHS
ID : R35 HL139598
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM119197
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL076136
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL128264
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001442
Pays : United States
Organisme : NCI NIH HHS
ID : R37 CA225655
Pays : United States
Organisme : NHLBI NIH HHS
ID : P01 HL142494
Pays : United States
Organisme : NHLBI NIH HHS
ID : R00 HL129168
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.
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